Metabolic Alcaloses

Metabolic AlcalosesDefinition and diagnosis:


A metabolic alkalosis is defined by the association of an alkaline blood pH ( > = 7.43) with an increase in the alkaline reserve ( > = 28 mmol / L).

Metabolic alkalosis results in an increase in PaCO 2(compensating alveolar hypoventilation), and a decrease in PaO 2 proportional to the increase in PaCO 2 .Chloraemia is lower than would be expected from the increase of HCO 3- with a small TrA bound to lactic acid production


Clinical signs are non-specific and inconstant. They associate: neurological signs if the pH is greater than 7.5: agitation, confusion, coma, epilepsy; neuromuscular signs: cramps, myoclonus (secondary to the fall of ionized calcium); of cardiac signs: arrhythmias.

Clinical approach:


The two conditions necessary to create a metabolic alkalosis are the entry of HCO 3- in the extracellular area by loss of acid or alkaline gain, which will generate alkalosis, and an increase in the capacity of the kidney to be reabsorbed the HCO 3- , which will maintain the alkalosis.


The entry of HCO 3- into the extracellular area may be renal or digestive. An entry of renal origin of the HCO 3 isobserved in the cases of primal hyperaldosteronism (Conn’s syndrome for example), or in case of influx of Na + in the distal nephron in the presence of hyperaldosteronism (treatment with diuretics of the loop), hyperaldosteronism being secondary to volleic depletion.

These two situations will combine three factors: a high Na + intake in the cortical collector tube; a hypermineralocorticism, the secretion of aldosterone becoming independent of the extracellular volume; a hypokalaemia, a consequence of the first two phenomena.

The influx of Na + into the cortical collector tube, while aldosterone is elevated, increases the secretion of H + . Indeed, aldosterone activates the Na + / K + ATPase and promotes the opening of the epithelial canal of the main cells. In the presence of Na + in tubular light, Na + is exchanged for H + and K + , resulting in alkalosis and hypokalaemia.Hypokalemia aggravates alkalosis because it increases distal acid secretion.

The loss of acid through the gastrointestinal tract during vomiting (rich in HCl) leads to the addition of HCO 3 in the extracellular sect, but in order to maintain alkalosis, renal reabsorption of HCO 3 – be increased.


Three mechanisms account for the maintenance of alkalosis: the dehydration of the extracellular sector which is the main factor, hypokalaemia, hypermineralocorticism.

Dehydration of the extracellular area decreases the rate of glomerular filtration and therefore the amount of 3- filtered HCO, which limits their renal excretion. In addition, the reabsorption of HCO 3- is increased in the proximal tube.

Hypokalemia also decreases the glomerular filtration rate and stimulates the distal secretion of H + by NH 4 + .

Hypermineralocorticism is a maintenance factor because it stimulates H + secretion if Na + delivery is maintained in the cortical collector tube.


The clinical consequences of metabolic alkalosis are still poorly understood but probably deleterious. In addition to depression in respiratory centers, alkalosis depresses tissue oxygenation by increasing the affinity of oxygen for hemoglobin and by generalized arterial vasoconstriction. Coronary or cardiac complications have been reported in patients with metabolic alkalosis.


The etiologies of metabolic alkaloses are divided into two groups: alkaloses associated with extracellular dehydration, and alkaloses associated with normal extracellular hydration or extracellular hyperhydration.


It is the cause of the maintenance of alkalosis in these etiologies.

The analysis of Na + and Cl  urinary makes it possible to distinguish the different causes. In some situations, such as vomiting associated with an unavowed intake of diuretics, for example, urinalysis can be difficult.

High urinary excretion of Na + and Cl -:

Alkalosis is initiated by a loss of H + by the kidney: treatments in progress by loop diuretics or thiazides; Bartter’s syndrome; Gitelman syndrome; deficiency in magnesium: alkalosis is not systematic and is generally moderate.

Its determinism is unknown. Rarely, alkalosis is triggered by an entry of HCO 3- in the extracellular area of ​​digestive or bone origin. The etiologies are hypercalcemia of nonparathyroid origin: Burnett syndrome occurring in patients with renal insufficiency consuming large quantities of calcium carbonate (calcium carbonate) salts, vitamin D intoxication, granulomatosis (sarcoidosis) and cancerous lysis of cancers .

Urinary excretion of Cl  and elevated Na +:

Alkalosis is triggered by loss of H + through the gastrointestinal tract:

– active vomiting or nasogastric suction;

– chronic diarrhea and villous tumors. In general, they are accompanied by acidosis, but sometimes an alkalosis is observed, of an indeterminate mechanism: an abnormality of the Cl  / HCO 3- exchanger in the ileum and the jejunum? Influence of hypokalaemia? Concomitant use of diuretics in the case of laxative disease?

õ Low urinary excretion of Cl  and Na +

Alkalosis is triggered by a loss of H + either by the digestive tract in case of vomiting in the recent past, or by the kidney in the case of diuretic treatment in the recent past and in the case of posthypercapital alkalosis. The latter is explained by the accumulation of HCO 3- while the patient was hypercapnic (metabolic compensation of respiratory acidosis).

The accumulation of HCO 3 leads to a deficiency of Cl  by chloruria.

When the alveolar ventilation is restored, the kidney can not excrete all accumulated HCO 3 due to the NaCl deficiency.

These metabolic alkaloses must be treated with NaCl, which allows to restore the hydration of the extracellular sector and thus renal excretion of HCO 3

 accumulated. Depletion in K + also contributes to the maintenance of alkalosis. It must also be compensated, but it is the intake of NaCl which constitutes the basic treatment.


This type of alkalosis is always related to a renal loss of acid by mineralocorticoid hyperactivity. Alkalosis is maintained by the maintenance of mineralocorticoid activity in spite of the volume expansion (which allows Na + to be added to the collecting tube) and by hypokalaemia which stimulates the excretion of H + .

The renin and aldosterone assays make it possible to differentiate three groups of etiologies.

Primary hyperaldosteronism.

In these situations, renin is low and non-stimulable, and high aldosterone: Conn’s disease, bilateral adrenal hyperplasia, adrenal cancer, hyperaldosteronism suppressible by dexamethasone. The latter affects the translocation of the 11-beta-hydroxylase gene to the 18-beta-hydroxylase gene, which makes the synthesis of aldosterone dependent on adrenocorticotrophic hormone (ACTH). Prescribing small doses of corticosteroids corrects high blood pressure (HTA) and hypokalemic alkalosis.

– Secondary hyperaldosteronism.

Before affirming secondary hyperaldosteronism, it must be ensured that the patient is not dehydrated, possibly by a perfusion of saline serum. In these situations, renin and aldosterone are elevated: renal artery stenosis, renin secreting tumor, accelerated or malignant hypertension.

– Hypermineralocorticism without aldosterone.

The mineralocorticoid activity is not related to aldosterone but to other normally inactive adrenal hormones (cortisol), or in quantities usually insufficient to exert a mineralocorticoid effect.

In these situations, renin and aldosterone are low: Cushing’s syndrome and treatment with corticosteroids, glycyrrhizin (licorice) poisoning, congenital adrenal hyperplasia of enzyme deficiencies, familial 11-beta-hydroxy-steroid dehydrogenase deficiency, Liddle’s syndrome (this is a mutation of the epithelial sodium channel, which increases its Na + reabsorption activity, resulting in hypertension with hypokalemic alkalosis).

All these causes of metabolic alkalosis must be treated with KCl, which restores the renal excretion of accumulated HCO 3- .

Finally, the alkalosis of K + deficits is explained by the transfer of H + to the intracellular medium and the increase of renal excretion of H + in the form of NH 4 + .

The contraction alkalosis is observed in the case of treatment with furosemide (Lasilix t ) which subtracts liquid from the extracellular area while the stock of HCO 3 remains constant.


The treatment of a metabolic alkalosis is first of all that of its maintenance factor, then that of its cause. Symptomatic treatment is only necessary in rare circumstances.


It is paramount. Treatment depends on the etiology:

– intake of NaCl in all situations associated with extracellular dehydration. It is the treatment of alkaloses by hypercalcemia, by vomiting or chronic diarrhea, etc .;

– intake of K + in all situations associated with extracellular hyperhydration. It is the treatment of alkaloses by primitive hyperaldosteronism, Cushing’s disease, etc.


Each cause of metabolic alkalosis has its own treatment. These include:

– stop thiazide or loop diuretics;

– ablation of a gastric tube or prescription of antisecretory if maintenance of the probe is necessary;

– the surgical treatment of an adenoma of Conn, etc.


In view of the clinical consequences of alkalosis, symptomatic treatment is only necessary in certain patients:

– respiratory distress patients in whom the correction of alkalosis may improve alveolar ventilation;

– patients with unstable angina or recent myocardial infarction;

– patients with neurological symptoms.

Ammonium chloride (NH 4 Cl) can be used either orally or by venous route. Hydrochloric acid (HCl), 0.15 or 0.25 N, can be perfused on a central pathway. These acids are contraindicated in patients with renal or hepatic impairment.Arginine hydrochloride was discontinued due to the possibility of severe hyperkalaemia. Antialdosterone (spironolactone: Aldactone t ) or K + saving diuretics (amiloride: Modamide t ) are good treatments for alkalosis in hyperaldosteronism.

Acetazolamide (Diamox t ) is not very effective and can increase PaCO 2, especially in respiratory insufficiency.